Review

Nutrition and cognition across the lifetime: an overview on epigenetic mechanisms

  • Received: 22 April 2021 Accepted: 12 July 2021 Published: 15 July 2021
  • The functioning of our brain depends on both genes and their interactions with environmental factors. The close link between genetics and environmental factors produces structural and functional cerebral changes early on in life. Understanding the weight of environmental factors in modulating neuroplasticity phenomena and cognitive functioning is relevant for potential interventions. Among these, nutrition plays a key role. In fact, the link between gut and brain (the gut-brain axis) is very close and begins in utero, since the Central Nervous System (CNS) and the Enteric Nervous System (ENS) originate from the same germ layer during the embryogenesis. Here, we investigate the epigenetic mechanisms induced by some nutrients on the cognitive functioning, which affect the cellular and molecular processes governing our cognitive functions. Furthermore, epigenetic phenomena can be positively affected by specific healthy nutrients from diet, with the possibility of preventing or modulating cognitive impairments. Specifically, we described the effects of several nutrients on diet-dependent epigenetic processes, in particular DNA methylation and histones post-translational modifications, and their potential role as therapeutic target, to describe how some forms of cognitive decline could be prevented or modulated from the early stages of life.

    Citation: Arianna Polverino, Pierpaolo Sorrentino, Matteo Pesoli, Laura Mandolesi. Nutrition and cognition across the lifetime: an overview on epigenetic mechanisms[J]. AIMS Neuroscience, 2021, 8(4): 448-476. doi: 10.3934/Neuroscience.2021024

    Related Papers:

  • The functioning of our brain depends on both genes and their interactions with environmental factors. The close link between genetics and environmental factors produces structural and functional cerebral changes early on in life. Understanding the weight of environmental factors in modulating neuroplasticity phenomena and cognitive functioning is relevant for potential interventions. Among these, nutrition plays a key role. In fact, the link between gut and brain (the gut-brain axis) is very close and begins in utero, since the Central Nervous System (CNS) and the Enteric Nervous System (ENS) originate from the same germ layer during the embryogenesis. Here, we investigate the epigenetic mechanisms induced by some nutrients on the cognitive functioning, which affect the cellular and molecular processes governing our cognitive functions. Furthermore, epigenetic phenomena can be positively affected by specific healthy nutrients from diet, with the possibility of preventing or modulating cognitive impairments. Specifically, we described the effects of several nutrients on diet-dependent epigenetic processes, in particular DNA methylation and histones post-translational modifications, and their potential role as therapeutic target, to describe how some forms of cognitive decline could be prevented or modulated from the early stages of life.


    Abbreviations

    AD

    Alzheimer's disease

    ALS

    Amyotrophic Lateral Sclerosis

    BDNF

    Brain-Derived Neurotrophic Factor

    BMI

    body mass index

    CBP

    CREB-binding protein

    CNS

    Central Nervous System

    DHA

    docosahexanoic acid

    DNMT

    DNA methyl-transferase

    DOHaD

    Developmental Origin of Health and Disease

    EGCG

    epigallocatechin gallate

    ENS

    Enteric Nervous System

    EPA

    eicosapentaenoic acid

    FAS

    fetal alcoholic syndrome

    FASD

    fetal alcohol spectrum disorders

    FTD

    Frontotemporal Dementia

    HATs

    histone acetyl-transferases

    HCY

    homocysteine

    HDACs

    histone deacetylases

    HMTs

    histone methyl-transferases

    IGF-2

    Insulin-like growth factor-2

    LCPUFAs

    long chain polyunsaturated fatty acids

    LOAD

    late onset Alzheimer's disease

    MCI

    mild cognitive impairment

    MeCP2

    methyl-CpG-binding protein

    PD

    Parkinson's disease

    POHaD

    Paternal Origin of Health and Disease

    RAR-α

    retinoic acid receptor-α

    SAH

    S-adenosyl-homocysteine

    SAM

    S-adenosyl-methionine

    SCFAs

    short-chain fatty acids

    VAD

    vitamin A deficiency

    VDR

    vitamin D receptor.

    加载中

    Acknowledgments



    This study was supported by funding from the Project “Bando Ricerca Competitiva 2017”, University of Naples Parthenope (D.R.289/2017) to L.M. and from the Department of Humanities, University of Naples Federico II (Fondi ricerca dipartimentale 2020 and 2021) to L.M.

    Conflict of interest



    All authors declare no conflicts of interest.

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